Excision of selectable genes from transgenic goat cells by a protein transducible TAT-Cre recombinase

Xu, Yuanyuan; Liu, Siguo; Yu, Guohua; Chen, Jianquan; Chen, Juan; Xu, Xujun; Wu, Youbing; Zhang, Aimin; Dowdy, Steven F.; Cheng, Guangcun

doi:10.1016/j.gene.2008.04.020

Cited by 24 publications

(23 citation statements)

References 28 publications

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“…Several reports have provided proof of concept for the potential of site-specific recombination technology for livestock genome engineering [65,[148][149][150]. Generation of marker-free cattle [14,151] and goats [152] originated from cells that were selected and subsequently subjected to recombinase-mediated marker removal has been documented ( Table 3).…”

Section: Application Of Site-specific Recombinasesmentioning

confidence: 99%

Exogenous enzymes upgrade transgenesis and genetic engineering of farm animals

Bosch

Forcato

Alustiza

et al. 2015

Cell. Mol. Life Sci.

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Transgenic farm animals are attractive alternative mammalian models to rodents for the study of developmental, genetic, reproductive and disease-related biological questions, as well for the production of recombinant proteins, or the assessment of xenotransplants for human patients. Until recently, the ability to generate transgenic farm animals relied on methods of passive transgenesis. In recent years, significant improvements have been made to introduce and apply active techniques of transgenesis and genetic engineering in these species. These new approaches dramatically enhance the ease and speed with which livestock species can be genetically modified, and allow to performing precise genetic modifications. This paper provides a synopsis of enzyme-mediated genetic engineering in livestock species covering the early attempts employing naturally occurring DNA-modifying proteins to recent approaches working with tailored enzymatic systems.

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Section: Application Of Site-specific Recombinasesmentioning

confidence: 99%

Exogenous enzymes upgrade transgenesis and genetic engineering of farm animals

Bosch

Forcato

Alustiza

et al. 2015

Cell. Mol. Life Sci.

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“…To confirm that mesothelial EMT could be enhanced by Notch signaling, we locally activated Notch signaling within the lung mesothelial cells in organ culture using a recombinant Crerecombinase fused to the HIV-TAT peptide (TAT-Cre) (Shaw et al, 2008;Xu et al, 2008). To induce constitutive Notch activity in labeled mesothelial cells, we cultured embryonic lungs from E14.5 Rosa N1ICD-GFP (Murtaugh et al, 2003) or Rosa EYFP mice (in which Cre activity will delete a loxP-flanked stop segment, resulting in expression of N1ICD::GFP or YFP, respectively) with 5 M TAT-Cre for 5 hours.…”

Section: Lung Mesothelial Cells Contribute To Mesenchyme Via Notch-trmentioning

confidence: 99%

Canonical Notch signaling in the developing lung is required for determination of arterial smooth muscle cells and selection of Clara versus ciliated cell fate

Morimoto

Liu

Cheng

et al. 2010

Journal of Cell Science

208

115

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SummaryLung development is the result of complex interactions between four tissues: epithelium, mesenchyme, mesothelium and endothelium. We marked the lineages experiencing Notch1 activation in these four cellular compartments during lung development and complemented this analysis by comparing the cell fate choices made in the absence of RBPj, the essential DNA binding partner of all Notch receptors. In the mesenchyme, RBPj was required for the recruitment and specification of arterial vascular smooth muscle cells (vSMC) and for regulating mesothelial epithelial-mesenchymal transition (EMT), but no adverse affects were observed in mice lacking mesenchymal RBPj. We provide indirect evidence that this is due to vSMC rescue by endothelial-mesenchymal transition (EnMT). In the epithelium, we show that Notch1 activation was most probably induced by Foxj1-expressing cells, which suggests that Notch1-mediated lateral inhibition regulates the selection of Clara cells at the expense of ciliated cells. Unexpectedly, and in contrast to Pofut1-null epithelium, Hes1 expression was only marginally reduced in RBPj-null epithelium, with a corresponding minimal effect on pulmonary neuroendocrine cell fate selection. Collectively, the primary roles for canonical Notch signaling in lung development are in selection of Clara cell fate and in vSMC recruitment. These analyses suggest that the impact of ␥-secretase inhibitors on branching in vitro reflect a non-cell autonomous contribution from endothelial or vSMC-derived signals.

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“…[32][33][34][35] Although the actual mechanism by which TAT and other CPPs deliver their cargo is not yet certain, it is definitely established that TAT is able to translocate proteins into the cell nucleus 36 and that translocated proteins retain their functional activity as demonstrated by ability of TAT-CRE to induce DNA recombination. 37,38 Given these issues and opportunities, we asked whether TAT-mediated transduction of NF-Ya peptide to human HSCs can stimulate their proliferation. We chose to use transcriptional activation of HOXB4 as one marker for biochemically active TAT-NF-Ya, and used in vitro cell growth, clonogenic assay, and in vivo transplantation to measure functional progenitor cell proliferation.…”

mentioning

confidence: 99%

TAT-mediated transduction of NF-Ya peptide induces the ex vivo proliferation and engraftment potential of human hematopoietic progenitor cells

Domashenko

Danet-Desnoyers

Aron

et al. 2010

Blood

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IntroductionThe ability of hematopoietic stem cells (HSCs) to sustain hematopoiesis throughout life involves the coordinated interaction of several genes and signaling pathways, including HoxB4, Notch1, Bmi-1, and Wnts. [1][2][3][4][5][6][7][8][9][10][11] Manipulating the levels of expression of one or more of these genes offers the potential to artificially alter the balance of stem cell proliferation versus differentiation for analytic and therapeutic applications.We previously identified the trimeric transcription factor Nuclear Factor Y (NF-Y) as a regulated activator of HoxB4 transcription, as well as several other genes involved in HSC proliferation, including HoxC4, HoxD4, Notch1, and Lef-1, and suggested that NF-Y is a candidate key regulator of HSC self-renewal. 12 NF-Y is composed of 3 subunits: NF-Ya, NF-Yb, and NF-Yc. NF-Yb and NF-Yc are constitutively expressed in most cells and interact via a histone-fold motif to form heterodimers. When NF-Ya peptide is expressed, trimers form that bind to a subset of CCAAT consensus binding site. [13][14][15][16][17] NF-Y regulates the expression of many genes important in diverse cell types, including the cell cycle control genes cyclin A2, cyclin B1, and cyclin B2, 18 and some erythroidspecific genes 19,20 MDR1 21 and GADD45 ␥. 22 Cellular, molecular, and developmental specificity for NF-Y activity is established through multiple mechanisms. In addition to the regulation of transcription, direct interaction of NF-Y with other transcription factors into larger-order transcription units plays a key role. Probably because of the importance of NF-Y in diverse cellular processes, constitutive deletion of NF-Ya in embryonic stem cells results in early embryonic lethality. 23 NF-Y plays an essential role in hematopoiesis through the regulated expression of NF-Ya. Postnatal deletion of NF-Ya within HSCs leads to a G2M block in HSCs and hematopoieitic progenitor cells, resulting in complete hematopoietic failure. 24 NF-Ya is preferentially expressed in HSCs and declines with their differentiation. Retroviral overexpression of NF-Ya in HSCs activates the transcription of genes implicated in self-renewal and differentiation, including the Hox4 paralogs HoxB4, HoxC4, and HoxD4, as well as Hes-1, LEF1, Notch1, p27, and telomerase, and biases HSCs toward self-renewal rather then differentiation, showing a prominent increase in their in vivo repopulating ability after bone marrow transplantation. 12 Although retroviral expression of NF-Ya is efficient and powerful, its application to clinical therapeutics is problematic because of both the difficulty in controlling the level and duration of expression of the transgene and the potential for insertional leukemogenesis. Dogs and macaques transplanted with primary CD34 ϩ cells transduced by retroviral vector overexpressing HoxB4, developed myeloid leukemia 2 years after transplantation. 25 These results suggest that viral delivery of genes biasing cells to undifferentiated state poses a significant threat of complications.Nonvira...

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Excision of selectable genes from transgenic goat cells by a protein transducible TAT-Cre recombinase

Cited by 24 publications

References 28 publications

Exogenous enzymes upgrade transgenesis and genetic engineering of farm animals

Exogenous enzymes upgrade transgenesis and genetic engineering of farm animals

Canonical Notch signaling in the developing lung is required for determination of arterial smooth muscle cells and selection of Clara versus ciliated cell fate

TAT-mediated transduction of NF-Ya peptide induces the ex vivo proliferation and engraftment potential of human hematopoietic progenitor cells

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